Download PDF by Frederick J. Suchy, Ronald J. Sokol, William F. Balistreri: Liver Disease in Children

By Frederick J. Suchy, Ronald J. Sokol, William F. Balistreri

ISBN-10: 0511286457

ISBN-13: 9780511286452

ISBN-10: 0521856574

ISBN-13: 9780521856577

Thoroughly revised re-creation of the most well known reference on pediatric liver affliction. Liver ailment in young ones, third version offers authoritative insurance of each element of liver affliction affecting babies, little ones, and teenagers. Chapters are written through foreign specialists and tackle the original pathophysiology, manifestations, and administration of those problems within the pediatric inhabitants. The 3rd version has been completely up to date and lines new contributions on liver improvement, cholestatic and autoimmune issues, fatty liver illness, and inborn mistakes of metabolism. a necessary source for all physicians excited about the care of kids with liver affliction.

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Extra resources for Liver Disease in Children

Sample text

Initiation of mammalian liver development from endoderm by fibroblast growth factors. Science 1999;284:1998–2003. 18. Deutsch G, Jung J, Zheng M, et al. A bipotential precursor population for pancreas and liver within the embryonic endoderm. Development 2001;128:871–81. 19. Serls AE, Doherty S, Parvatiyar P, et al. Different thresholds of fibroblast growth factors pattern the ventral foregut into liver and lung. Development 2005;132:35–47. 20. Miller DL, Ortega S, Bashayan O, et al. Compensation by fibroblast growth factor 1 (FGF1) does not account for the mild phenotypic defects observed in FGF2 null mice.

At 7 weeks of gestation, hematopoietic cells outnumber hepatocytes. Primitive hepatocytes are smaller than mature cells and are deficient in glycogen. As the fetus nears term, hepatocytes predominate and enlarge with expansion of the endoplasmic reticulum and accumulation of glycogen. Hepatic blood flow, plasma protein binding, and intrinsic clearance by the liver (reflected in the maximal enzymatic and transport capacity of the liver) also undergo significant postnatal maturation [1]. These changes correlate with an increased capacity for hepatic metabolism and detoxification.

1 shows the postnatal development of several of the more important CYP450 enzymes. The CYP3A subfamily is the most abundant of the CYP enzymes, involved in the metabolism of approximately 50% of commonly used medications [43,44]. CYP3A7, the major fetal hepatic cytochrome (30–50% of total liver P450), is uniquely present during organogenesis, and it is involved in steroid metabolism [45]. Expression declines after the first postnatal week and is nondetectable in most livers by 1 year of age. Variably detectable in the fetus, CYP3A5 is expressed at significant levels in about half of all children [46].

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Liver Disease in Children by Frederick J. Suchy, Ronald J. Sokol, William F. Balistreri


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